The overall objective of these studies is to quantitate the reserve capacity of the endothelial fluid pump. Clinical studies have indicated that the failure of this pump to compensate for increases in endothelial permeability, as occurs in Fuchs for example, is responsible for the corneal edema noted in these patients. The limited reserve capacity of the endothelial pump could thus be a primary factor in the development of corneal edema. These studies, aimed at quantitating alterations in endothelial pump function at the membrane level, will further our understanding of adaptive mechanisms and physiologic reserve of the endothelial pump. These studies will employ the specific binding of tritiated ouabain to endothelial Na/K ATPase to quantitate alterations in pump site density and distribution. ATPase activity will be assayed using the 32P-ATP assay. These data will be correlated to the physiologic evaluation of endothelial function (in vitro perfusions) and endothelial morphology (light histology and wide-field specular microscopy). Answers will be sought to the following questions: 1) Are changes in endothelial pump function associated with in vivo wound healing? 2) How do the density, distribution and activity of Na-K pump sites in cultured corneal endothelial cells compare to fresh tissue? And, are changes in these parameters associated with the establishment of an intact (contact inhibited) monolayer? 3) Do changes in Na-K pump and barrier functions occur in stored corneal endothelium? 4) What is the density of Na-K pump sites in other transporting ocular tissues (ciliary body and lens epithelium)?